Platelet activation takes place after
attachment and adhesion events or after other stimuli
that triggeres activation mechanisms such as thromboxane
A2, ADP, thrombin or PAF (platelet activating factor,
released from endothelial cells, PMN or monocytes).

In a first step of activation, platelets undergo shape
change, cytoskeleton rearrangement and organelle centralization.
Release of dense granule contents (ADP and ATP) and
serotonin, occurs. In a second step, there is alpha
granule release of fibrinogen, fibronectin and vWF,
exposure of fibrinogen and fibronectin receptors on
platelet surface, and finally, release of arachidonic
acid to be converted to thromboxane A2, which is a powerful
mediator of platelet aggregating response.

Cyclooxygenase is the key enzyme responsible
for synthesis of thromboxane A2 in platelets. Aspirin
and other anti-inflammatory drugs interfere with an
early step of prostaglandin pathway, suppressing the
formation of pro-aggregatory cyclic endoperoxides precursors
of thromboxane A2.

The following animations show detailed
information on most of the receptors, molecular mechanisms,
signaling pathways and platelet responses that are triggered
after activation, as well as their regulatory and modulatory
mechanisms: